Effects of urea, trimethylamine oxide, and osmolality on respiration and citrulline synthesis by isolated hepatic mitochondria from Squalus acanthias

The aims of this study were to determine the pathway of swelling-activated trimethylamine oxide (TMAO) efflux and its regulation in spiny dogfish ( Squalus acanthias) red blood cells and compare the characteristics of this efflux pathway with the volume-activated osmolyte (taurine) channel present in erythrocytes of fishes. The characteristics of the TMAO efflux pathway were similar to those of the taurine efflux pathway. The swelling-activated effluxes of both TMAO and taurine were significantly inhibited by known anion transport inhibitors (DIDS and niflumic acid) and by the general channel inhibitor quinine. Volume expansion by hypotonicity, ethylene glycol, and diethyl urea activated both TMAO and taurine effluxes similarly. Volume expansion by hypotonicity, ethylene glycol, and diethyl urea also stimulated the activity of tyrosine kinases p72syk and p56lyn, although the stimulations by the latter two treatments were less than by hypotonicity. The volume activations of both TMAO and taurine effluxes were inhibited by tyrosine kinase inhibitors, suggesting that activation of tyrosine kinases may play a role in activating the osmolyte effluxes. These results indicate that the volume-activated TMAO efflux occurs via the organic osmolyte (taurine) channel and may be regulated by the volume activation of tyrosine kinases.

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Renal Conservation of Trimethylamine Oxide by the Spiny Dogfish, Squalus Acanthias

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1958.194.2.229 ◽

1958 ◽

Vol 194 (2) ◽

pp. 229-235 ◽

Cited By ~ 39

Author(s):

Julius J. Cohen ◽

Marcus A. Krupp ◽

Charles A. Chidsey

Keyword(s):

Renal Tubule ◽

Narrow Range ◽

Plasma Concentrations ◽

Squalus Acanthias ◽

Spiny Dogfish ◽

Trimethylamine Oxide

Trimethylamine oxide (Oxide) plasma concentrations in the dogfish have been found to be maintained within the narrow range of 60–80 µmol/ml. These levels are maintained in spite of prolonged (up to 41 days) fasting. The Oxide is freely filterable at the glomerulus but is avidly reabsorbed by the renal tubule. Thus, less than 10% of the filtered Oxide appears in the urine. Dogfish urine has been found to contain an unidentified volatile amine, not NH3, presumed to be trimethylamine. The possible role of the Oxide in elasmobranch physiology is discussed.

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Trimethylamine oxide (TMAO) decreases stress‐induced alteration of Hsp70 production and organic acid transport by the choroid plexus (CP) of the dogfish shark, Squalus acanthias

The FASEB Journal ◽

10.1096/fasebj.20.5.a1238-d ◽

2006 ◽

Vol 20 (5) ◽

Author(s):

Alice R. A. Villalobos ◽

Jennifer Higgins ◽

Brendan Vosburgh ◽

J. Larry Renfro

Keyword(s):

Organic Acid ◽

Choroid Plexus ◽

Squalus Acanthias ◽

Acid Transport ◽

Trimethylamine Oxide ◽

Dogfish Shark ◽

Organic Acid Transport

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Effect of trimethylamine and its homologues on renal conservation of trimethylamine oxide by the spiny dogfish, Squalus acanthias

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1958.196.1.93 ◽

1958 ◽

Vol 196 (1) ◽

pp. 93-99 ◽

Cited By ~ 5

Author(s):

Julius J. Cohen ◽

Marcus A. Krupp ◽

Charles A. Chidsey ◽

Charles I. Biltz

Keyword(s):

Specific Effect ◽

Tubular Secretion ◽

Tubular Reabsorption ◽

Urine Flow ◽

Squalus Acanthias ◽

Weak Base ◽

Physiological Regulation ◽

Trimethylamine Oxide ◽

Renal Tubular Reabsorption ◽

Renal Tubular

In renal clearance experiments with dogfish, trimethylamine HCL (TMA) administration (i.m.) results in a large increase in trimethylamine oxide (Oxide) excretion. This is shown to occur by inhibition of net renal tubular reabsorption of the Oxide. The TMA, on the other hand, reaches the urine by net tubular secretion in quantities which are consistent with the attainment of diffusion equilibrium across the pH gradient between urine and plasma. The effect of TMA is not related to increased urine flow but is a specific effect on Oxide reabsorption. The administration of the homologue of TMA, dimethylamine, results in a similar but less profound blockade of Oxide reabsorption. Methylamine, however, has no effect at all on Oxide reabsorption. Large excretory losses of TMAO occurred without any change in TMAO plasma level, further indicating the physiological regulation of the plasma concentration of this weak base.

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